The results show that 1 tablet of Quick-eze is most effective in neutralizing the stomach because the number of moles of HCl reacted with the NaOH is 0.00216 moles (one tablet), which is less than Gaviscon. The number of moles of NaOH that were added from the burette is 0.00327 moles (one tablet of Gaviscon). However, the actual number of moles of calcium carbonate in a Gaviscon tablet is 0.0019 moles, but for Quick-eze, the number of moles is 0.0079 moles (actual amount of base in both tablets). This means that the number of moles added from the burette was more compared to the actual amount, which affects the accuracy of the results. However, these results are somewhat precise because of the minor difference between the experiment results …show more content…
For example; for every trial, different volumes of NaOH was dispensed (different titre values) for every trial for Quick-eze ant-acid tablet, 18.3ml was the titre value in the first trial. However, for the second trial, 22.3ml volume of NaOH dispensed with the tablet and the HCl acid, as shown in the results (page 4, table 2) due to the error occurred, such as misreading the volume, indicator error and misinterpretation. Hence, this error affected the credibility of the results because the titre values are not concordant (Quick-eze), which then affected the number of moles of hydrochloric acid neutralised by the antacid tablet. Additionally, shortage of the standardized solutions (HCl and NaOH) is a systematic error because people were rushing due to the time provided and the concentration of HCl and NaOH is different might differ (might not prepared to 0.1M …show more content…
It is an indirect technique, where reagent 1 (ant-acid tablet) reacts with excess reagent 2, the analyte (HCl) in reaction, where some reagent 2 remains in the solution and the sodium hydroxide is the titrant (reactant 3). For example; a known mass of the Gaviscon ant-acid tablet dissolves in an excess known volume and concentration of HCl and reacts. Then, the remaining amount of HCl acid will be titrated with a known concentration of sodium hydroxide to a phenolphthalein endpoint. By performing this experiment, the amount of excess acid will be determined and then the amount of HCl acid reacted with the ant-acid tablet will be calculated. Aim The purpose of this experiment is to determine the most effective commercial ant-acid tablet in neutralising the Gastric acid by using the back-titration technique. Hypothesis It is hypothesised that Quick-eze (ant-acid) tablet will be the most effective antacid tablet in neutralizing the gastric acid because of its active ingredients. The actual amount of base (Carbonate) in both
1. To titrate a hydrochloric acid solution of “unknown” concentration with standardized 0.5M sodium hydroxide.
Antacids are medicines that can be bought over-the-counter which are taken by mouth and can help to quickly relieve acidic refluxes in the body.https://en.wikipedia.org/wiki/Antacid The major symptom of gastroesophageal reflux disease (GERD), are taste of acid, bad breath, chest pains, etc. GERD is a long term condition where stomach contents come back up into the esophagus. Complications include esophageal strictures and Barrett’s esophagus.https://en.wikipedia.org/wiki/Gastroesophageal_reflux_disease An Esophageal Stricture is a narrowing or tightening of the esophagus that causes swallowing difficulties.
6M H.Cl will be used to substitute the Stomach Acid, as the buffer for a reaction to occur.
The second system we will cover is the Gastrointestional System. All medications in this system were used based upon the manufacturers intended use as referenced by Davis’s Drug Guide. The first medication she was put on relating to the GI system is polyethylene glycol which was used to draw water into the lumen of the GI tract and aid in the evacuation of the GI tract without causing electrolyte imbalance. The teaching that was given to her for this medication was to take the medication until gone even if she is feeling better, avoid alcohol and products that contain aspirin or NSAIDs and to avoid foods that may cause an increase in GI irritation. She was also told to report any black and tarry stools, diarrhea or abdominal pain immediately. The second medication she was put on relating to the GI system was furosemide which was used to prevent edema and encourage excretion of sodium and water (Valerand, 2013). We informed her that she should not double the doses, and that if she started to get a rash, muscle weakness, cramps, nausea, diaainess, numbness or tingling she needed to contact the physician immediately. The final
Activated charcoal is the gastrointestinal decontamination technique that should be used in this patient to help adsorb to any NSAID that hasn’t been absorbed since a large amount was consumed.
absorption of acetaminophen has a pKa of 9.5 and in the alkaline medium of the duodenum
Therefore, somatostatin works inhibiting the acid secretion acting directly in the parietal cell and in that same way blocking the regulation of gastrin and histamine (Washington.edu, n.d.). Additionally, somatostatin can also inhibit other gastrointestinal hormones like vasoactive intestinal polypeptide (VIP) and cholecystokinin (CCK) (Utiger, 2011). The clinical use of somatostatin as a drug to reduce the production of gastric acid it is limited due to two critical factors: first, somatostatin has a very short half-life with less than three minutes of action and second, somatostatin can only be produced by the body (Huang, 1997). However, some studies suggest the use of somatostatin analogues in the treatment of reduction of gastric acid. According to Ritz, et al., (1999) Vapreotide, a somatostatin analog was used as testing trial to treat intragastric acidity without positive outcome in the regulation of acidity and mediation of gastrin. Also, they found that Vapreotide can also diminish the contraction of the gallbladder reducing the effects of the biliary functions (Ritz, et al.,
GLP-1 receptor agonists slow the digestive process and help lower glucose, though less than sulfonylureas. These medicines include Exenatide and Liraglutide, they come with a possibility of nausea, but worse, a risk of pancreatitis.
The PPIs are inactive pro drugs that are carried in the bloodstream to the parietal cells in the gastric mucosa. The pro drugs readily cross the parietal cell membrane in the cytosol. These drugs are weak bases and therefore have a high affinity for acidic environments. They diffuse across the secretory membrane on the parietal cell into the extracellular secretory canaliculus, the site of active proton pump. Under this acidic conditions the prodrugs are converted to their active form, which irreversibily binds the proton pump, inhibiting acid secretions. Since the’ active principles ‘ forms at a low pH it concentrates selectively in the acidic enviorment of the proton pump and results in extremely effective inhibition of acid secretion.The different PPIs(Omeprazole,Esomeprazole,Lanzoprazole, Pantoprazole and Rabeprazole ) bind to different sites on the proton pump, which may explain their differences in potency on a milligram per milligram basis.
Explanations for the fast rise in occurrence of EAC involve the increasing prevalence of gastroesophageal reflux and obesity as well as the declining incidence of Helicobacter pylori infection. Helicobacter pylori infection is correlated with hypergastrinemia, the excess of gastrin in the blood. Gastrin is a hormone that is secreted by G cells situated in the gastric antrum and works on the parietal cells to trigger the production of hydrochloric acid. Constant hypergastrinemia due to daily PPI therapy contributes to the raised gastric acid-secretory capacity that is not obvious throughout PPI therapy, but that emerges quickly when the drug is stopped. Increased acid production due to hypergastrinemia poses a risk factor for development of
The ulcer protective effect of SANGU PARPAM III was studied as per the method of Shay et al., (1945).The ulceration is caused by accumulation of acidic gastric juice in the stomach and by this method several parameters can be estimated.
According to clinical studies, the TZDs mainly lower fasting and postprandial glucose concentrations as well as free fatty acid concentrations. Most studies also indicated that there is a decrease in insulin concentrations. The fact that the TZDs act as insulin sensitizers has been confirmed by direct measurements in in vivo studies in humans.12
The build up of stomach acid may cause irritation and excess pain to individuals. Luckily, antacids being a weak base can help relieve the symptoms and pain. Antacids, such as Gelusil, Medi-Firs, Alka Seltzer, and Alcalak are neutralizing agents of acids that become helpful to the human body when heartburn occurs. Heartburn, also known as acid reflux is a common medical issue that occurs when hydrochloric acid (HCl) from the stomach moves backward along the digestive track to the esophagus (located within the throat). This reverse flow of fluids causes a burning sensation due to and possible sour taste that is characteristic of acids [1].
In vitro: Ebrotidine had an anti secretory potency comparable to that of ranitidine and about 10-fold greater than that of cimetidinep, and had greater affinity for H2 receptors than these agents. Ebrotidine could also reduce parietal cell secretion of hydrochloric acid by inhibiting the gastric cellular response to histamine. Moreover, ebrotidine maintained mucosal cellular integrity and prevented cellular calcium imbalance by inhibiting EGF-stimulated calcium channel protein phosphorylation
Add 5mL of gastric juices (contains both pepsin solution and HCl) to test tube 3